FIGURE 5.

Role of group 1 mGluR, glia, and TNF in the learning deficit. (A) Spinally transected rats received the group 1 mGluR1 antagonist CPCCOEt (i.t.; 100 nmol), or its vehicle, prior to VIS (Shock). Instrumental learning was tested 24 h later. Prior exposure to shock inhibited learning (Vehicle-Shock). Pretreatment with CPCCOEt blocked the induction of this learning impairment (CPCCOEt-Shock). (B) Rats were pretreated with the PKC inhibitor BIM (i.t.; 0.023 nmol), or its vehicle, and then received an injection of the group 1 mGluR agonist DHPG (100 nmol) or saline. Administration of DHPG alone (Vehicle-DHPG) impaired learning and this effect was blocked by pretreatment with BIM (BIM-DHPG). (C) Subjects received an intrathecal injection of LPS (100 μg), or its vehicle. The next day, a TNF inhibitor (sTNFR1; 700 ng) or vehicle was given intrathecal and subjects were tested in the instrumental learning paradigm. Prior treatment with LPS impaired learning (LPS-Vehicle). Administration of sTNFR1 prior to testing eliminated the learning deficit (LPS-sTNFR1). (D) Rats received an intrathcal injection of TNF (6000 pg) or its vehicle. The next day, they were given the GluR2 antagonist Naspm (i.e., 10 mM) or vehicle and tested in the instrumental learning paradigm. Rats that had previously received just TNF (TNF-Vehicle) failed to learn. This learning impairment was blocked by Naspm (TNF-Naspm). Adapted from Ferguson et al. (2008) and Huie et al. (2012a).